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SPINA BIFIDA

 Description: A central nervous system defect results from failure of the neural tube to
close during embryonic development generally in the lumbosacral region
 Causes:
 Actual cause is unknown; multiple factors
 Genetic – if a sibling has had neural tube defect
 Environmental factors
 Medications, viral infection and radiation
 Types:
1. Spina bifida occulta- Posterior vertebral arches fail to close in the lumbosacral
area.
 Spinal cord and meninges remains in the normal anatomic position
 Defect may not be visible dimple or a tuff of hair on the spine
 Asymptomatic may have slight neuromuscular deficits
 No treatment if asymptomatic aimed at specific symptoms

2. Spina bifida cystica- Protrusion of the spinal cord and/or its meningeswith varying
degrees of nervous tissue involvement.
a) Meningocele
 part of spinal protrudes through opening in the spinal canal
 sac is covered with thin skin no nerve roots involved
 no motor or sensory loss Good prognosis after surgery

b) Myelomeningocele (meningomyelocele)
 with spinal nerves roots in the sac
 have sensory or motor deficit
 below site of the lesion
 80% have multiple handicaps

 Assessment- Depends on the spinal cord involvement


1. Visible spinal defect
2. Motor/sensory involvement
a) Flaccid paralysis of the legs
b) Altered bladder and bowel function
c) Hip and joint deformities
d) Hydrocephalus

 Diagnostics:
 Prenatal- ultrasound, amniocentesis (MAFP)
 Postnatal
 xray of spine
 ct scan
 myelogram-uses a special dye and an X-ray (fluoroscopy) to provide a
very detailed picture of the spinal cord and spinal column
 encephalogram
 urinalysis, BUN, Creatinine clearance

 Management:
1. Surgery- closure of sac within 48 hours, shunt, orthopedic
2. Drug therapy- Antibiotic, Anticholinergic

 Nursing Management:
1. Prevent trauma to the sac
a) cover with a sterile, moist (normal saline), non adherent dressing
b) change the dressing every 2 to 4 hours as prescribed, keep area free
from contamination
c) place in a prone position to minimize tension on the sac
d) head is turned to one side for feeding
e) Administer meds
2. Prevent Complication
a) Use aseptic technique to prevent infection.
b) Assess the sac for redness, clear or purulent drainage, abrasions,
irritation, and signs of infection.
c) Clean intermittent catheterization
d) Perform neurological assessment
e) Assess for physical impairments such as hip and joint deformities
3. Provide adequate nutrition
4. Provide sensory stimulation
5. Provide emotional support to parents and family
6. Provide discharge teachings
 wound care
 ROM, PT
 signs of complications
 medication regimen
 positioning – feeding ,diaper change

HYDROCEPHALUS (738-744)

Normal Physiology:
CSF forms in 1st & 2nd ventricles of brain aqueduct of Sylvius and 4th ventriclesubarachnoid
space of spinal cord (absorption)

 Description: An imbalance of cerebrospinal fluid (CSF) absorption or production


caused by: malformations, tumors, hemorrhage, infections, or trauma
 Accumulation of excess CSF in subarachnoid space & 4th ventricles
 Maybe related to myelomeningocele
 If PRETERM from intraventricular hemorrhage
 Maybe a result of:
 Aqueductal stenosis
 Blockage of CSF outflow from 4th ventricles
 Results in head enlargement (cranial sutures not firmly knitted + pressure from excess
fluid) and increased ICP
 Types:
 COMMUNICATING (extravascular)- occurs as a result of impaired absorption
within the subarachnoid space.
 Fluid is able to reach spinal cord
 NONCOMMUNICATING (intravascular)- blockage in the ventricular system
that prevents CSF from entering the subarachnoid space
Reasons for CSF Accumulation:
 Overproduction of fluid from choroid plexus in 1st/2nd ventricle as could occur from tumor
 Obstruction of passage
o Narrow aqueduct Sylvius (common)
o Narrow foramina of Magendie and Luschka—opening allowing fluid to leave 4th
ventricle
o Hemorrhage leaving adhesions
o Arnold-Chiari Disorder (elongation of lower brain stem and displacement of 4th
ventricle into upper cervical canal
o Dandy-Walker cyst (fluid filled sack by one of the ventricles in the brain)
 Interference with CSF absorption
o Maybe d/t sgxal removal of portion of subarachnoid membrane s/t meningocele
or extensive subarachnoid hemorrhage

 Assessment:
1. Increased head circumference
2. Thin, widely separated bones of the head that produce a cracked pot sound
(Macewen's sign) on percussion
3. Anterior fontanel tense, bulging, and no pulsating; sutures will separate prior
to fontanel bulging
4. Dilated scalp veins
5. Sunsetting eyespressure on CN 3,4,6 forces the eyes downward revealing a
rim of sclera above iris
6. Behavior changes, such as irritability and lethargy
7. Headache on awakening
8. Nausea and vomiting
9. Ataxia- lack of coordination of muscle movement
10. Nystagmus- involuntary movement of the eyes
11. Late signs: High, shrill cry and seizures.
12. Decreased RR,PR; Increased BP/Temp
13. Normal intelligence
14. Affected fine motor development

 Diagnostic Test: CT scan, MRI, Skull X-ray


 Transillumination- holding a bright light such as a flashlight or specialized light
(Chun gun) against the skull in a darkened room; a skull filled with fluids rather
than solid brain substance

 Management - treatment depends to cause

Surgical interventions
 GOAL: Prevent further CSF accumulation by bypassing the blockage and
draining the fluid from the ventricles to a location where it may be reabsorbed.
 Ventriculoperitoneal shunt -the CSF drains into the peritoneal cavity
 Atrioventricular shunt -CSF drains into the right atrium of the heart
 Destruction of portion of choroid plexus
 Shunt revisions may be necessary as child grows
 ALTERNATIVE: ENDOSCOPIC THIRD VENTRICULOSTOMY
 Small opening in the floor of third ventricle to allow CSF to bypass fourth
ventriclereturn to circulation to be absorbed

Acetazolamide (diamox)- promote the excretions of excess fluids


Shunting—threading polyethylene cath under skin from ventricles to peritoneum
 Preoperative interventions
 Monitor I&O
 Give SFF as tolerated until a preoperative NPO status is prescribed.
 Reposition head frequently and use an egg crate mattress under the head
to prevent pressure sores.
 Prepare the child and family for diagnostic procedures and surgery
 Postoperative interventions
 Monitor VS (!!Inc Temp/BP, Dec PR/RR) and neurological signs.
 Position the child on the unoperated side
 Observe for signs of increased ICP
o elevate head 15-30 degrees (enhances gravity flow through shunt)
 Monitor for signs of infection
 Measure head circumference.
 Provide comfort measures; expected level of functioning
 Administer medications as prescribed, diuretics, antibiotics, or
anticonvulsants.
 Instructions on parents re: wound care, shunt revision
 Availability of support groups; community agencies
 Note for three incision sites
o Behind ear
o Neck (helps thread cath)
o Abdomen
 Instruct the parents on how to recognize shunt infection or malfunction
o In an infant- irritability, lethargy, and feeding poorly
*a high shrill cry maybe a sign of ↑ICP
o In a toddler- headache and a lack of appetite
o In older children- an alteration in the child's level of consciousness.
 Adequate nutrition to prevent Constipationincreased ICP &
possible compression of shunt
NDx: Risk for ineffective cerebral tissue perfusion r/t ↑ICP; Risk for imbalanced nutrition, less
than body req, r/t inc ICP

LARGE FOR GESTATIONAL AGE (694-695)


1. Description: Neonate who is plotted at or above the 90 th percentile on the intrauterine growth
curve
2. Weigh more than 4,000 grams
3. Immature Development
4. Cause – unknown (genetic factors and maternal conditions)
 Maternal diabetes – is the most widely known contributing factor
 Causes overproduction of nutrients and GH
 Increase insulin acts as a fetal growth hormone
 Macrosomia – an unusually large newborn with birth weight of more than 4500grams
 Beckwith-Wiedermann syndrome—general body overgrowth and congenital anomalies
Assessment
5. large, obese
6. Lethargic and limp
7. May feed poorly
8. Immature
9. Sign and symptoms of birth trauma
 Bruising
 Broken clavicle
 Evidence of molding
 Cephalhematoma
 Caput succedaneum

Problems of LGA babies


1. Hypoglycemia (low blood sugar) of baby after delivery
2. Respiratory distress
a. Possible pressure on respiratory center
3. Hyperbilirubinemia
a. d/t absorption of blood from bruising during delivery & breakdown of extra RBC
created by polycythemia
4. Potential complications related to increase in body size:
a. Leading cause of breech position and shoulder dystocia
b. Fractured skull, clavicles, cervical or brachial plexus injury
and erb’s palsy

Management
Routine newborn care with special emphasis on the following:
a) Monitor vital signs frequently, especially respiratory status. (diaphragmatic paralysis d/t
edema of phrenic nerve)
b) Monitor blood glucose levels and for signs of hypoglycemia
c) Initiate early feedings
d) Note any signs of birth trauma or injury
e) Monitor for infection and initiate measures to prevent sepsis
f) Provide stimulation, such as touch and cuddling.

SEPSIS
 Description: Generalized infection resulting from the presence of bacteria in the blood
 Major common cause is group B beta- hemolytic streptococci
 Contributing factors:
1. Prolonged rupture of membranes
2. Prolonged or difficult labor
3. Maternal infection
4. Cross contamination
5. Aspiration
 Assessment findings – often does not have specific sign of illness
1. Poor feeding
2. Irritability
3. Lethargy
4. Pallor
5. Tachypnea
6. Tachycardia
7. Abdominal distention
8. Temperature instability – difficulty keeping temperature within normal range
 Diagnosis:
1. Blood, urine, and cerebrospinal fluid cultures
2. Routine CBC, urinalysis, fecalysis
3. Radiographic test
 Management
1. Intensive antibiotic therapy
2. IV fluids
3. Respiratory therapy
 Nursing interventions- Routine newborn care with special emphasis on the following:
1. Monitor vital signs, assess for periods of apnea or irregular respirations.
 If apnea, stimulate by rubbing chest or foot
2. Administer oxygen as prescribed
3. Provide isolation as necessary- Monitor and limit visitors
4. Handwashing before after handling neonate

PRETERM NEWBORN
Description: A neonate born before 37 weeks of gestation
Primary concern relates to immaturity of all body systems
Cause: unknown
Maternal factors: age, smoking, poor nutrition, Placental problem , Preeclampsia/ eclampsia
Fetal factors: multiple pregnancy, infection
Other factors: poor socioeconomic status, environmental exposure to harmful substance

Assessment
 Respirations are irregular with periods of apnea
 Body temperature is below normal
 Skin is thin, with visible blood vessels and minimal subcutaneous fat pads, may
appear jaundiced (Poikilothermic-easily take on the temperature of the environment)
 Poor sucking and swallowing reflexes
 Bowel sounds are diminished

Common or special problem of preterm neonates


1. Respiratory Distress Syndrome
 Hyaline membrane disease
 due to lung immaturity; deficient in surfactant
2. Hyperbilirubinemia
 high level of bilirubin in the blood,
 neonate become jaundice due to immaturity of the liver
 Kernicterus--staining of brain cells with bilirubin, causing irreversible brain damage
3. Infection - not able to receive IgG globulins
4. Cold stress-less subcutaneous tissue, poikilothermic
5. Anemia – less iron stores

Management
1. Improving respiratory function- Oxygen therapy, Mechanical ventilator
2. Maintaining body temperature- Isolette – maintains ideal temperature, humidity and oxygen
concentration isolates infant from infection, Kangaroo Care
3. Preventing infection- Handwashing
4. Promoting nutrition- Gavage feeding, Milk feeding
5. Promoting Sensory stimulation- Gentle touch, speaking gently and softly, music box or
low tuned radio

Nursing Interventions
1. Monitor vital signs every 2 to 4 hours
2. Administer oxygen and humidification
as prescribed.
3. Monitor intake and output
4. Monitor daily weight.
5. Maintain newborn in a warming device.
6. Reposition every 1 to 2 hours,and handle newborn carefully
7. Avoid exposure to infections.
8. Provide newborn with appropriate stimulation, such as touch
9. Suctioning of secretions as needed
10. Monitor for signs of infection
11. Provide skin care
12. Provide complete explanations for parents

DIFFERENCES PRETERM FULL TERM


Posture “Relaxed attitude” limbs more extended More flexed attitude
Ear Ear cartilages are poorly developed, Well formed cartilages
may fold easily
Sole Only fine wrinkles Well and deeply creased
Female genitalia Clitoris is prominent; labia majora Clitoris is not as prominent; labia
poorly developed majora fully developed
Male genitalia Scrotum is under developed and not Scrotum is fully developed,
pendulous, with minimal rugae pendulous, rugated
Scarf sign Elbow is easily brought across the With resisting attempt when elbow
(placing hand to chest with little or no resistance is brought to the midline of the
opposite shoulder chest
posteriorly)
Grasp reflex Weak Strong, allowing the infant to be
lifted up from the mattress

POST-TERM NEWBORN
Description: Neonate born after 42 weeks of gestation
About 12% of all infants are post-term
Causes of delayed birth is unknown
Maternal factors: First pregnancies between the ages 15 to 19years
Woman older than 35 years
Multiparity
Fetal factors: Fetal anomalies such as anencephaly

Assessment
 Depleted subcutaneuos fat: old looking “old man facies”
 Parchment-like skin (dry,wrinkled and cracked) without lanugo
 Fingernails long and extended over ends of fingers
 Abundant scalp hair
 Long and thin body
 Sign of meconium staining
 Nails and umbilical cord (yellow to green)

COMPLICATIONS OF POST MATURITY


1. The placenta begins to aged toward the end of pregnancy, and may not function as
efficiently as before.
2. The failing placental function will place infant at risk for intrauterine hypoxia during labor and
delivery.
3. MECONIUM ASPIRATION SYNDROME
4. HYPOGLYCEMIA - FROM NUTRITIONAL DEPRIVATION AND POOR STORAGE OF
GLYCOGEN AT BIRTH
5. POLYCYTHEMIA- increase RBC
Management
1. Ultrasound is done to evaluate fetal development, amount of amniotic fluids and the placenta
signs of aging
2. To reduce the chance of meconium aspiration, upon delivery of newborn’s head and just
before the baby takes his first breath suctioning of the mouth and nose is done

Nursing management
1. Closely monitor the newborn cardiopulmonary status
2. Administer supplemental oxygen therapy as needed
3. Frequent monitoring of blood sugar; assess for sign of hypoglycemia
4. Provide thermoregulated environment– use of isolette or radiant heat warmer
5. Monitor for signs of meconium aspiration syndrome

INTUSSUSCEPTION (1275-1276)
 Invagination or telescoping of a portion of the small intestine into a more distal segment of
the intestine (at juncture of distal ileum and proximal colon)
 3 times more likely in boys than girls and the common cause of intestinal obstruction in childhood
 Cause is unknown
 Factors:
a) Hyperperistalsis and unusual mobility of cecum and ileum
b) Lesion such as polyp, tumor,
c) Hypertrophy of Peyer’s Patcheslymphatic tissue that inc size upon viral infection
d) Meckel’s diverticulum
 It is considered a surgical abdominal emergency in children
 Mechanical Bowel Obstruction Occurs: intestinal walls press against each other causing
inflammation, edema and decreased blood flow.
 May progress to necrosis, perforation and peritonitis- gangrene of the bowel
S/Sx: elevated temp, peritoneal irritation, inc WBC, rapid pulse

 Clinical presentation
1. Sudden onset of abdominal pain ( in a healthy baby) q15-20 mins
2. Infant cries out sharply and draws knees up to abdomen
3. Vomiting occurs and increases overtime (Bile stained vomitus)
 d/t obstruction is below amplulla of Vater—point where bile empties into
duodenum begins
4. Currant jelly stoolblood + mucus
5. Signs of shock - Rapid weak pulse, pallor, marked sweating
6. Positive (+) for occult blood in stools
7. Sausage-shaped mass in RLQ

 Diagnosis- Often based on history and physical examination alone + xray for confirmation
1. Barium Enema- is definitive (in 75% of cases); It is therapeutic and curative in most
cases with less than 24-hour duration.
2. Digital rectal exam - reveals mucous, blood

 Immediate treatment
1. IV fluids
2. NPO status
3. Diagnostic barium enema
 Surgery
1. Manual Reduction of invagination
2. Resection with anastomosis
3. Possible colostomy (gangrenous)
 Nursing management
1. Provide routine pre- and post operative care for abdominal surgery
2. Monitor fluid and electrolyte status
3. Maintain nutrition and hydration
4. Resume feedings 24 hrs post operative (best if bowel sounds return)
5. Observe 24hrs p-op as recurrence of intussusception may occur additional reduction or
surgery
Ndx: Pain r/t abn peristalsis; risk for deficient fluid volume r/t bowel obstruction

HIRSCHSPRUNG’S DISEASE (1283-1284)


 Also known as – Aganglionic megacolon
 Absence of ganglion cells in a portion of the large intestine (usually at lower sigmoid
colon, above the anus)
 Is a parasympathetic nerve cells that regulates peristalsis in the intestine
 The absence of the ganglion cells would result to absence peristalsis and affected colon
becomes dilated and Filled with feces and gas
 Area proximal to obstruction dilates leading to abdominal distention
 Caused by abnormality in Chromosome 10
 The disease may be a familial congenital defect or may be associated with other anomalies,
such as Down syndrome and genitourinary abnormalities.

 Assessment findings
1. S/sx do not become apparent until 6-12months of age
2. Thin and malnourished with large, distended abd
3. No BM more than once a week with ribbon like or watery stools
NEWBORN CHILDREN
◦ Failure to pass meconium ◦ Failure to gain weight and
stool delayed growth
◦ Refusal to suck ◦ Abdominal distention
◦ Abdominal distention ◦ Vomiting
◦ Bile-stained vomitus ◦ Constipation alternating with
diarrhea
◦ Ribbon-like and foul-smelling
stools

 Diagnostic studies:
1. Rectal biopsy
 Shows lack of innervations
2. Anorectal manometry
 Tests the strength or innervation of internal rectal sphincter by inserting
balloon cath & measuring pressure exerted
3. Rectal exam
 Rectum is empty compared to constipation (in which hard cracked stools
are present)
4. Barium Enema
 ! may not be expelled
5. USD with contrast medium
 Outlines narrow, nerveless portions; distended portion

 Management
1. Surgery
 Temporary colostomy- A portion of the large intestine is brought through the
abdominal wall to carry stool out of the body
 Bowel repair- Dissection and removal of the affected section with
anastomosis of intestine
 aka Abdominal – perineal pull through; pull-through procedure

Done in 2 parts
 Temporary ColostomyBowel repair by 12-18 months of age
2. Daily Isotonic enema
3. Drug therapy - Antibiotic, Stool softeners
4. Diet therapy- Low residue diet
 Low-fiber, high-cal, high-CHON

Nursing Management
5. Administer enema as ordered; Isotonic solution only
 Hypotonic (tap water) solution can cause death d/t cardiac congestion, cerebral
edema
 Moves rapidly to intestinalinterstitial/intravascular
compartmentsequalize osmotic pressures
6. Do not treat loose stools – child is constipated
7. Administer TPN
8. Instruct parents on colostomy care, correct diet

Post-op
1. Observe for abd distention
2. Assess bowel sounds
3. Observe for flatus and stools
4. Peristalsis
a. Remove NGT
b. SFF
i. Fluids
ii. Full Fluids
iii. SD
iv. Minimal residue diet
v. Normal diet for age

Ndx: Imbalanced nutria, less, r/t reduced bowel movement; Constipation (r/t reduced bowel fnx)
CELIAC DISEASE (1280-1281)
 Gluten-Induced Enteropathy
 Malabsorption Syndrome
 Celiac Sprue
 Is a sensitivity or immunologic response to protein, particularly the gluten factor of protein found in
grains of wheat, barley, rye, and oats
 results in the accumulation of the amino acid - glutamine, which is toxic to intestinal mucosal cells.
 Intestinal villi atrophy occurs, which affects absorption of ingested nutrients.

Gluten ingestion atrophy//flattening of villi at SI prevents absorption of foodssteatorrhea, failure to


thrive, malnutrition

Classic Sign: Thin child with distended abdomen

 Assessment
1. Acute or insidious diarrhea
2. Steatorrhea
3. Anorexia
4. Abdominal pain and distention
5. Muscle wasting, particularly in the buttocks and extremities
6. Vomiting
7. Anemia
8. Irritability

Celiac Crisis
 Precipitated by infection, fasting, ingestion of gluten
 Extreme and acute profuse watery diarrhea and vomiting occurs
 Can lead to electrolyte imbalance, rapid dehydration, severe acidosis
 Intensive therapy to replace fluids and electrolytes is required

Dx:
 History taking (s/sx usually appear by 6-18 months—period in which gluten is introduced to
diet)
 Serum Analysis of antibodies
o Endomysial antibody, Tissue transglutaminase is obtained
 Biopsy of intestinal mucosa via endoscopy
 Observance of child by placing in gluten-free diet
o (+) dramatic changes: gain wt, steatorrhea improves, irritability fades

 Interventions
1. Maintain a gluten-free diet, substituting corn, rice, and millet as grain sources.
2. Instruct parents and child about lifelong elimination of gluten sources such as wheat, rye, oats,
and barley.
3. Administer mineral and vitamin supplements, including iron, folic acid, and fat-soluble
supplements A, D, E, and K
4. Teach the child and parents about a gluten-free diet and about reading food labels carefully for
hidden sources of gluten
5. Instruct the parents in measures to prevent celiac crisis.

 Basics of a Gluten-Free Diet


 FOODS ALLOWED
o Meat such as beef, pork, and poultry and fish, eggs, milk and dairy products,
vegetables, fruits, rice, corn, gluten-free wheat flour, puffed rice, cornflakes,
cornmeal, and precooked gluten-free cereals
 FOODS PROHIBITED
o Commercially prepared ice cream, malted milk, prepared puddings,grains,
including anything made from wheat, rye, oats, or barley, such as breads, rolls,
cookies, cakes, crackers, cereal, spaghetti, macaroni noodles& beer

RESPIRATORY DISTRESS SYNDROME (RDS)


 Description: Serious lung disorder caused by immaturity and inability to produce surfactant,
resulting in hypoxia and acidosis
 Surfactant – a biochemical compound that reduces surface tension inside the air sac
 Usually forms by 34 weeks gestation
 Prevents alveolar collapse upon expiration
 Decrease in surfactant results to lung collapse, thus greatly reducing infant’s vital supply of
oxygen
 Damaged lung cells combines with other substance present in the lungs to form fibrous
substance called hyaline membrane (Hyaline membrane disease)
 this membrane lines the alveoli and blocks gas exchange in the alveoli

 Assessment
1. Expiratory grunting –major- is the body's way of trying to keep air in the lungs so they will
stay open
2. Tachypnea
3. Nasal flaring
4. Sternal, Subcostal Retractions
5. Seesaw – like respirations (chest wall retracts and the abdomen protrudes)
6. Decreased breath sounds
7. Apnea
8. Pallor and cyanosis
9. Hypothermia
10. Pneumothorax
11. CXR—radiopaque areas
12. ABG—respiratory acidosis

 Management
a) Oxygen therapy- hood, nasal prong, mask, endotracheal tube, CPAP (Continuous
Positive Airway Pressure) or PEEP (Positive End –Expiratory Pressure) may be
used
 CPAP/PEEP—exerts pressure to alveoli during expiration to prevent collapse +
supply O2
 !!! watch out for ROP & Bronchopulmonary dysplasia
b) Muscle relaxants – Pancuronium (Pavulon)
 Reduces muscular resistance
 Prevents pneumothorax
 Prepare Atropine or Neostigmine Methylsulfate
c) Liquid Ventilation- Uses perfluorocarbons – substances used in industry to assess
leaks
 Reversed I/E ratio of 2:1 for ventillators
d) Nitric Acid- Causes pulmonary vasodilation – increases blood flow to the alveoli
 No decrease in systemic vascular tone
 Forms methomoglobin (combined hgb + drug)—causes the vasodilation
 Redirects pulmonary blood by dilating pulmonary arterioles
e) Extracorporeal membrane oxygenation (ECMO)
 Means for oxygenation

 Nursing Interventions
1. Monitor color (cyanosis), respiratory rate, and degree of effort in breathing.
2. Support respirations as prescribed
3. Monitor arterial blood gases and oxygen saturation levels
 (arterial blood gases from umbilical artery).so that oxygen administered to the
newborn is at the lowest possible concentration necessary to maintain adequate
arterial oxygenation.

SEIZURE
 Recurrent sudden changes in consciousness, behavior, sensations and or muscular activities
beyond voluntary control cause by excess neuronal discharge
 Normally the neuron send out messages in electrical impulses periodically and the firing
individual neuron is regulated by an inhibitory feedback loop mechanism
 with seizures many more neurons than normal fire in a synchronus fashion in a particular
area of the brain; the energy generated overcomes the inhibitory feedback mechanism
 Febrile seizures is common in children between 6mos – 3yrs old
 common in 5% of population under 5 years old, familial
 Nonprogressive, does not generally result in brain damage
 Seizures occur only when fever is rising
 Commonly associated with high fever – 38.9 to 41.1 celsus
 Some appear to have a low seizures threshold and convulse when a fever of 37.8 to
39.8
 Classification:
a) Partial seizure
 Simple – localized motor activity shaking of arm or leg limited to one
side of the body
 Complex – psychomotor (temporal lobe) seizure memory loss and
staring non purposeful movements

AURA – sensation that signals an attack


after – sleep or confuse; unaware of the seizure

b) Generalized (Status epilepticus)


 Tonic – clonic prodromal, AURA, tonic, post ictal
 Absence - rarely 20 seconds stares straight, does not fall
 Contributing factors:
 Intracranial infection
 Space occupying lesion
 CNS defects

 Assessment findings
 Restlessness / irritability
 Body stiffens and loss of consciousness
 Clonic movements – quick, jerking movements of arms, legs, and facial muscle
 Pupils dilate and roll up

 Diagnostic test:
 blood studies - to rule out lead poisoning,
 hypoglycemia
 infection
 Electrolytes imbalance
 EEG – to detect abnormal wave

 Treatment
a) Drug therapy- Diazepam, Phenobarbital, Dilantin
b) Surgery- tumor, hematoma

 Interventions
1. Reduce fever with antipyretics.
2. Give prescribed medication
3. Generalized seizure precautions
4. Do not restrain; pad crib rails; do not use tongue blade
5. Observe and record the time of seizure, duration, and body parts involved.
6. Suction and administer oxygen after the seizure as required.
7. Observe the degree of consciousness and behavior after seizure
8. Provide rest after the seizure

CLEFT LIP AND PALATE


 Nonunion of the tissue and bone of the upper lip and hard/soft palate during embryonic
development
 Failure of the maxillary and pre maxillary processes to fuse during fetal development
 Etiology – primarily genetic; environmental factors
a) Viral infection exposure to radiation
b) Folic acid deficiency
c) Teratogenic factors
 Assessment findings
1. Facial abnormality
2. Difficulty sucking and swallowing
3. Milk escapes through nose
 Assessment
1. Cleft lip - can range from a slight notch to a complete separation from the floor of the
nose.
2. Cleft palate
 nasal distortion
 midline or bilateral cleft
 variable extension from the uvula and soft and hard palate.
 Associated problems
1. Feeding problems
2. URTI
3. Ear infection
4. Speech defect, dental malformation
5. Body image
 Management – Rule of Ten
1. Surgical correction
 Cheiloplasty – correction of cleft lip
 Palatoplasty – cleft palate surgery done –before speech development ; allow for
palatal changes
 Logan bar/ steri - strips – to take tension off on the sutures
2. Team approach therapy
 Dentist and orthodontist
 Audiologist
 Speech therapist
 Pediatrician
 Nursing Intervention
CLEFT LIP CLEFT PALATE
PRE OPERATIVE 1. Feed in upright position’ in 1. Prepare parents to care for child
small frequent feedings after surgery
2. Burp frequently 2. Instruct concerning feeding
3. Use large-holed nipples methods and positioning
4. Use rubber-tipped syringe – if
unable to suck
5. Gavage feeding as ordered
6. Finish feeding with water
7. Provide emotional support for
parents and family
POST 1. Maintain patent airway 1. Suction mucus and saliva gently
OPERATIVE 2. Assess color ; monitor for and do not touch the sutures
frequent swallowing 2. Incision care
3. Do not place in prone position 3. Clean suture with sterile cotton
4. Avoid straining suture lines swab with half strength hydrogen
5. Use elbow restraints peroxide followed by saline
6. Resume feedings as ordered 4. Apply antibiotic ointment
7. Provide pain control as ordered 5. Do not displace Logan bar
6. Do not place in prone position,
place in side lying position
7. Keep spoons, pacifier, straws,
away from child’s mouth for 7 to 10
days post op
8. Elbow restrain
9. Special feeder – syringe with
rubber tubing into side of mouth,
Breck feeder

MENINGITIS
 Description: inflammations of meninges of the brain and spinal cord
 Cause by bacteria, viruses, other microorganism
 as a primary disease or as a result of complications of neurosurgery, trauma,
infection of the sinus or ears, or systemic infections.
 H Influenzae Meningitis – the most common form; between 6 to 12 months
 Bacterial meningitis - Haemophilus influenza type B, Streptococcus pneumoniae,
or Neisseria meningitidis
 Viral meningitis is associated with viruses such as mumps, herpesvirus, and
enterovirus.
 Assessment
 Fever, chills, headache,
 high-pitched cry, irritability
Vomiting, Poor feeding or anorexia
Bulging anterior fontanel in the infant
Signs of meningeal irritations
 Nuchal rigidity – stiff neck
 Positive Kernig sign- Severe stiffness of the hamstring muscle causes
an inability to straighten the leg when the hip is flexed to 90 degrees.
 Opisthotonos
 arching of the back
 head and heels bent backward
 and body arched forward
 Brudzinski sign - Flexion at the hip in response to forward flexion of
the neck
 CSF by LP: increased WBC, Protein, dec glucose
 Interventions
1. Provide isolation and maintain it for at least 24 hours after antibiotics are
initiated.
2. Administer antibiotics and antipyretics as prescribed.
3. Perform neurological assessment and monitor for seizures and
complications
4. Assess for changes in level of consciousness and irritability.
5. Monitor intake and output.
6. Assess nutritional status.
7. Determine close contacts of the child with meningitis because the contacts will
need prophylactic treatment.
8. Meningococcal vaccine is recommended to protect against meningitis.

Possible NDx:
 Pain r/t meningeal irritation

 Risk for ineffective cerebral tissue perfusion r/t increased ICP


Outcomes:
o VS return to normal
o Alert and oriented
o Motor, cognitive, sensory fnx within acceptable parameters
o Specific gravity of urine is 1.003 to 1.030

Interventions:
 Observe for S/Sx of ↑ICP (↑BP,↓PR)
 Monitor IV infusion to prevent overhydration and ↑ICP
 Measure urine specific gravity to detect secretion of ADH d/t pituitary
pressure
 Measure head circumference and wt. daily
 Monitor hearing acuity which may be ↓ if there is compression of the 8th cranial
nerve.

OTITIS MEDIA
 bacterial or viral infection of the middle ear
 common in infants and preschoolers
 Eustachian is shorter, wider, and straighter- thereby, allowing nasopharyngeal secretion to enter
middle ear more easily
 Assessment findings
1. Behavior that would indicate pain
 restless and repeatedly shakes the head
 Frequently pulls or tugs at affected ear
2. Irritability, cough, nasal congestion, fever
3. Hearing impairment
4. Purulent discharges
 Diagnosis
1. Examination of ear with otoscope–reveal bright red bulging eardrum
2. culture and sensitivity of ear discharges
 Possible complication: permanent hearing loss mastoiditis
 Management
1. Antibiotics, analgesics
2. Myringotomy- incision into the tympanic membrane to relieve pressure and drain
the fluid with /without tube
 Postoperative interventions
 Wear earplugs while bathing, shampooing, and swimming,
 Diving and submerging under water are not allowed.
 Child should not blow his or her nose for 7 to 10 days after surgery.
 Interventions
1. Encourage fluid intake.
2. Teach the parents to feed infants in upright position, to prevent reflux.
3. Instruct the child to avoid chewing as much as possible during the acute period
because chewing increases pain.
4. Provide local heat and have the child lie with the affected ear down.
5. Instruct the parents in the appropriate procedure to clean drainage from the ear with
sterile cotton swabs.
6. Instruct the parents
 Administration of analgesics or antipyretics
 Administration of the prescribed antibiotics, emphasizing that the 10- to 14-day
period is necessary to eradicate infective organisms.
 Screening for hearing loss may be necessary.
7. Administering ear medications.
 Younger than age 3, pull the lobe down and back.
 Older than 3 years, pull the pinna up and back

IRON DEFICIENCY ANEMIA


 Hypochromic anemia: hgb inadequate, erythrocytes are pale(hypochromia); reduced in diameter
(microcytic); Poikilocytic (irregular shape)
 Iron stores are depleted, resulting in a decreased supply of iron for the manufacture of
hemoglobin in RBC
 Daily Fe requirement: 11-15 mg
 Usually occurs at 9m to 3y
 Causes: blood loss, increased metabolic demands, syndromes of GI malabsorption, dietary
inadequacy;
 Drinking more milk than iron
 Heavy menstruation
 Over weight d/t high CHO intake
 With GI problems
 Iron not digested
 With chronic diarrhea
 Not absorbed
 Parasitic infection
 GI tract lesions
 More common in:
 Child bearing women
 Poor iron intake
 Infants and children in rapid growth
 Pregnant/lactating mothers
 (N) NBs have enough iron stores for 6months; except:
 Preterms
 Iron are laid out during end of gestation
 At risk of IDA by 5-6 months
 Babies of mothers with IDA
 Give iron supplement by 2months

 Assessment:
 compensatory tachycardia
 Pallor
 Weakness, fatigue, irritability
 Lab results

 Pale conjunctiva
 “fair skinned”
 Poor muscle tone
 Reduced activity
 Heart enlarged
 Ausculatation: soft systolic precordial murmurs; tachycardia (as attempt supply cells
withO2)
 Possible spleen enlargement
 Fingernails: spoon shaped; depressed in contour
 Labs:
 dec Hgb: <11g/100ml
 reduced hct: below 33%
 Low Mean corpuscular level
 Low mean corpuscular hgb
 Low serum Fe
 Monoamine Oxidase absent
 Important for CNS maturation

 Management:
 Food choices: meats, dark green & leafy vegetables, egg yolks, liver, kidney beans, iron-
enriched formula & cereal
 Not more than 32oz of milk/day
 Administer iron (ferrous sulfate) supplements as prescribed
 4-6mg/kg/d (severe) 3mg/kg/d (moderate) for 4-6 weeks
 Give with vit c (Fe is best absorbed with acid
 Important to brush teeth
 If iron dextran, use z-track
 Teach parents to administer iron supplements:
 Between meals
 Give with Vit C
 Do not give with antacids or milk
 Oral care
 Side effects
ACUTE RHEUMATIC FEVER
 An inflammatory disorder that may involve the connective tissue of heart, joints, lungs and
brain
 Is an autoimmune disease that occurs as a reaction to a group A beta-hemolytic
streptococcal infection, pharyngitis
 Usually occurs by 6-15y
 recurring (no immunity to strep infections)
 It is precipitated by streptococcal infection which is undiagnosed and untreated
 Antigenic markers for streptococcal toxin closely resemble markers of the heart valves; this
resemblance causes antibodies made against the streptococcal to also attacks the heart valve
 Strep pharyngitis high antibody response10 days p, autoimmune response (takes
weeks) damages heart valves

 Assessment findings: Divided to major and minor symptoms according to Jones criteria
 to diagnose
 2 major symptoms
 1 major and two minor

 MAJOR SYMPTOMS:
 Carditis
 inflammation of the heart muscle around
 heart valves; aschoff’s nodules (lesions found in heart, brain, vessels)
 apical systolic murmur (from atrial insufficiency)
 Blowing, high frequency; transmits to axilla
 Polyarthritis/ Migratory polyarthritis-
 a temporary migrating inflammation of the large joints
 May be with fluid accumulation
 Chorea - Sydenham’s chorea; St.Vitus’ dance –
 A CNS disorder characterized by abrupt, purposeless involuntary movement
 Only in 10%
 Exacerbated by stress
 Results to dysfnx speech, facial grimace, poor hadn control
 Subcutaneous nodules –
 painless, firm collections of collagen fibers over bones or tendons
 Erythema marginatum -
 Macular found on trunk
 Infrequent, but definitve sign
 transient , non pruritic rash (resembles giraffe spots)
 To diagnose
 Presence of 2 of the major manifestation or
 one major manifestation plus 2 minor manifestations are present along with evidence of
streptococcal infections
 Exceptions are chorea and indolent carditis each of which by itself can indicate rheumatic
fever
 Clinical findings / minor manifestations
 Arthralgia
 Fever
 Laboratory findings
 Elevated Erythrocyte sedimentation rate
 Elevated C-reactive protein
 Elevate antistreptolysin O (ASO) titer
o dx for streptococcal infection
 ECG - Prolonged PR interval
o Not for dx, but evaluated heart involvement
 leukocytosis
 Evidence of previous group A streptococcal infection
  + Throat culture or rapid streptococcal antigen test

 Medical management
1. Drug therapy
a. Penicillin PO IM– used in acute phase
For 10 day course
- given as prophylactic until age 20 or for 5 years

- Erythromycin as substitute

b. Salicylates – analgesics, anti-inflammatory, antipyretic effect

c. Steroids – anti-inflammatory effect


used only in severe carditis and valve damage
Phenobarbitals; diazepam—reduces purposeless movements of chorea
Digoxin; diurectics-- CHF

2. Bed rest – is essential during the active process of rheumatic fever to reduce cardiac
workload

- 1 week to 6 months

 Selected Nursing Diagnosis


 Acute pain related to inflammatory process
 Deficient diversional activity related to prescribed bed rest
 Activity intolerance related to pain and fatigue
 Risk for injury related to involuntary movement
 Risk for noncompliance with prophylactic drug therapy related to financial or emotional
burden of lifelong therapy

 Whenever the child is to have oral surgery, including dental work, extra prophylactic
precaution should be taken, even in adulthood

POISONING
 Poison – any substance that is harmful to the body Ingestion of toxic substance
 Common agent in childhood – soaps, cosmetics, detergents or cleaner and plants
 Modes of exposure: ingestion, Inhalation, spray
 Signs and Symptoms
1. GI disturbances
 Vomiting, abdominal pain, anorexia
 distinctive odor
2. Respiratory /circulatory disturbances
 collapse , shock, unexplained cyanosis
3. CNS manifestation
 confusion
 disorientation
 sudden loss of conc
 convulsion
 General Interventions
1. Stabilize child’s condition patent airway
2. Prevent absorption
 Determine type of substance ingested
 Induced emesis –except caustic material ingestion, comatose, active seizure or
lacking gag reflex
 Syrup of ipecac
 Gastric lavage
 Activated charcoal
 Absorbs toxic substances that have been swallowed to prevent being
absorbed at stomach
 Cathartic
3. Provide treatment and prevention information to parents
4. Incorporate anticipatory guidance related to the developmental stage of the child
5. Discuss general first aid measures with parents
 Methods of prevention
1. Child proofing the environment
2. Educating parents and child
3. Anticipatory guidance
4. Understanding and applying the principles of G/D

 Specific Poisoning

1. Salicylate poisoning = aspirin, oils of wintergreen,


Toxicity begins at doses of 150 - 200 mg/kg.
S/S – CNS depression, vomiting, respiratory failure

2. Acetaminophen poisoning = commonly used analgesics


Toxic at 150mg/kg
Risk – liver damage
Antidote – mucomyst (N-Acetylcysteine)
Binds to breakdown product so that it will not bind to liver cells
S/S – vomiting, liver tenderness, abdominal pain
AST(SGOT), ALT(SGPT), liver enzymes rise

3. Lead poisoning- plumbism


 Toddlers / preschoolers
 Usually caused by paints
 Lead interferes with red blood cell function
 Blocks incorporation of Fe into protoporphyrin compound (makes up heme
unit)hypochromic, microcytic anemia
 Possible kidney destruction
 Excess excretion of AA, glucose, phosphates in urine
 Lead value of 15ug/dl – health hazard
 Symptoms appear when lead level is – 70ug/dl
 Most serious effect is lead encephalitis
 Dx: two successive episodes of serum level >4u/dl
Identified also through radiology of GI, longbones
 Affects IQ, cause learning disability, behavioral attention problems

 S/S
 Abdominal complaints – colicky pain, constipation, vomiting
 Pallor
 Irritability
 Loss of coordination
 Encephalopathy
 + lead in the blood

 Nursing action
 Administer chelating agents
o dimercaprol ( BAL in Oil ) not given if allergy w
peanuts(prepared in peanut oil solution
o edatate calcium disodium ( calcium EDTA)
 Provide nutritional counseling
 Aid in eliminating environmental conditions that led to lead ingestion
 INGESTION OF POISONS: LEAD
o When lead enters the body, it affects the erythrocytes, bones and
teeth, and organs and tissues, including the brain and nervous
system; the most serious consequences are the effects on the
central nervous system.
o Chelation therapy- removes lead from the circulating blood and
from some organs and tissues.
o Common route is hand to mouth from contaminated objects or from
eating loose paint chips, crayons, or pottery that contains lead.
o Blood lead level test: Used for screening and diagnosis
Less than 10 mcg/dL Reassess or rescreen in 1 year or sooner if exposure status changes.
10 to 14 mcg/dL Provide family lead education, follow-up testing, and social service
referral if necessary.
15 to 19 mcg/dL Provide family lead education, follow-up testing, and social service
referral if necessary; on follow-up testing, initiate actions for blood
lead level of 20 to 44 mcg/dL.
20 to 69 mcg/dL A blood lead level greater than 20 mcg/dL is considered acute; provide
coordination of care, clinical management, including treatment,
environmental investigation, and leadhazard control (the child must
not remain in a lead-hazardous environment if resolution is necessary).
70 mcg/dL or greater Medical treatment is provided immediately, including coordination of
care, clinical management, environmental investigation, and lead-hazard
control.

 Dimercaptosuccinic accid (DMSA)/succimer- for lead level of 10-20ug/100ml


 Dimercarpol (British anti-Lewiste BAL) or edetate calcium disodium (CaEDTA) for greater
than 45ug/100ml
o CaEDTA
 Given IV or IM
 Painful, combined with 0.5ml procaine
 Can lead to nephrotoxicity
 Monitor BUN, crea, protein in urine
 Monitor I&O
 S/E: removes calcium from body
o BAL
 Able to remove lead from blood and other tissues
 CaEDTA limited soft tissues and bones
 !danger of severe toxicity; only used on severe lead poisoning
 CI: peanut allergy, G6PD deficiency
 Do not give with iron

4. Caustic poisoning
 Ingestion of strong alkali (lye, bowl cleaners, hair care products)
 May cause burns and tissue necrosis in the mouth, esophagus, stomach
 S/S immediate pain, drooling d/t edema, mouth turns white, tachycardia/pnea,
pallor, hypotension
 DO NOT MAKE CHILD VOMIT. CAUSES ADDITIONAL BURNS
 DO NOT ADMINISTER ACTIVATED CHARCOAL- not effective, may block
endoscopic view
 Pharyngeal edema may cause airway obstruction – intubation might be necessary

Management
 (dilute corrosive with water or milk not more than 120cc)
 Relieve pain IV Morphine
 CXR
 Laryngoscopy/esophagoscopy asses damge to lungs and esophagus
 Assess VS (!RRassesses if edema in pharynx causes obstruction)
o Increases restlessness O2 deprivation
 Intubation/Tracheotomy !may cause further injury
 Proton Pump Inhibitorsprotects stomach reflux to burned esophageal area
TONSILLITIS AND ADENOIDITIS
 Tonsillitis refers to inflammation and infection of the tonsils (palatine).
 Adenoiditis refers to inflammation and infection of the adenoids (pharyngeal tonsils).

 Assessment
a. Persistent or recurrent sore throat
b. Enlarged, bright red tonsils that may be covered with white exudate
c. Difficulty in swallowing
d. Mouth breathing and an unpleasant mouth odor
e. Fever
f. Cough
g. Enlarged adenoids may cause nasal quality of speech, mouth breathing, hearing difficulty,
snoring, and/or obstructive sleep apnea.

 Preoperative interventions
1. Assess for signs of active infection.
2. Assess bleeding and clotting studies because the throat is vascular.
3. Prepare the child for a sore throat postoperatively, and inform the child that he or she will
need to drink liquids.
4. Assess for any loose teeth to decrease the risk of aspiration during surgery.

 Postoperative interventions
1. Position the child prone or side-lying to facilitate drainage.
2. Have suction equipment available, but do not suction unless there is an airway
obstruction.
3. Monitor for signs of hemorrhage (frequent swallowing may indicate hemorrhage); if
hemorrhage occurs, turn the child to the side and notify the physician.
4. Discourage coughing or clearing the throat.
5. Provide clear, cool, noncitrus and noncarbonated fluids.
6. Avoid milk products initially because they will coat the throat.
7. Avoid red liquids, which simulate the appearance of blood if the child vomits.
8. Do not give the child any straws, forks, or sharp objects that can be put into the mouth.
9. Administer acetaminophen (Tylenol) for sore throat as prescribed.
10. Instruct the parents to notify the physician if bleeding, persistent earache, or fever occurs.
11. Instruct the parents to keep the child away from crowds until healing has occurred.

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